Abstract
Background: Studies have shown an association between chronic rhinosinusitis (CRS) and non–cystic fibrosis (CF) bronchiectasis. Objective: We aimed to determine whether CRS increases the risk of developing non-CF bronchiectasis. Methods: A retrospective analysis was conducted utilizing electronic medical records from an academic center. Patients with CRS without bronchiectasis, with at least 1 chest computed tomography (CT) scan performed after the diagnosis of CRS, were identified between January 2006 and December 2015. Charts were reviewed until May 2022. The control group was age-, sex-, and race-matched, and included patients without CRS, asthma, or chronic obstructive pulmonary disease (COPD) who had at least 1 chest CT scan. Bronchiectasis was identified by chest CT radiology reports. The odds of developing bronchiectasis were analyzed in patients with CRS without asthma or COPD (cohort 1) and patients with CRS with asthma or COPD (cohort 2). Results: The odds of developing bronchiectasis were significantly higher in patients with CRS (139 of 1,594; 8.7%) than in patients in the control group (443 of 7,992; 5.5%; odds ratio OR 1.63; 95% confidence interval [95% CI] 1.34–1.99). Furthermore, the odds of developing bronchiectasis were higher in cohort 1 (63 of 863; 7.3%; OR 1.34; 05% CI 1.02–1.76) and cohort 2 (76/ of 731; 10.4%; OR 1.98; 95% CI 1.53–2.55) versus the control group. After adjusting for confounding diseases, the association was attenuated in cohort 1 (OR 1.22; 95% CI 0.92–1.61) but remained significant in cohort 2 (OR 1.78; 95% CI 1.37–2.31). Conclusions: The CRS is associated with the future development of non-CF bronchiectasis. Patients with CRS, especially those with asthma or COPD, have a higher likelihood of developing bronchiectasis than patients without CRS.
Original language | English (US) |
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Pages (from-to) | 3116-3122.e2 |
Journal | Journal of Allergy and Clinical Immunology: In Practice |
Volume | 12 |
Issue number | 11 |
DOIs | |
State | Published - Nov 2024 |
Funding
Conflicts of interest: D. B. Conley reports contact with Regeneron, Medtronic, and Intersect ENT. A. Kato reports a research grant from Regeneron Pharmaceuticals/Sanofi; and a research gift from Lyra Therapeutics. R. C. Kern serves as a consultant for Sanofi-Regeneron, GlaxoSmithKline (GSK) and Lyra Therapeutics. R. P. Schleimer reports consulting fees from Intersect ENT, Merck, GSK, Sanofi, AstraZeneca/Medimmune, Genentech, Actobio Therapeutics, Lyra Therapeutics, Astellas Pharma, Allakos, Otsuka, and Aqualung; receives royalties from Siglec-8 and Siglec-8 ligand-related patents licensed by Johns Hopkins to Allakos Inc. W. W. Stevens is consultant for GSK; and has served on advisory boards for Regeneron and Melinta. B. K. Tan reports personal fees from Sanofi Regeneron/Genzyme and GSK. A. T. Peters receives research support from Astra Zeneca and Sanofi Regeneron; and serves on the advisory board for GSK, Astra Zeneca, and Sanofi Regeneron. The rest of the authors declare that they have no relevant conflicts of interest. This study was funded by National Institutes of Health (NIH) grant number P01AI145818 (CRISP2).
Keywords
- Chronic rhinosinusitis
- Non–cystic fibrosis bronchiectasis
ASJC Scopus subject areas
- Immunology and Allergy